INT140295

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.64
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 5
Disease Relevance 5.70
Pain Relevance 0.44

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

mitochondrion (BCL2) cell morphogenesis (BCL2) endoplasmic reticulum (BCL2)
intracellular (BCL2) cytoplasm (BCL2) cytosol (BCL2)
Anatomy Link Frequency
cleavage 3
BCL2 (Homo sapiens)
Pain Link Frequency Relevance Heat
COX-2 inhibitor 104 97.04 Very High Very High Very High
cINOD 36 76.44 Quite High
metalloproteinase 3 75.00 Quite High
Inflammatory response 3 68.28 Quite High
Central nervous system 14 68.16 Quite High
Inflammation 81 63.84 Quite High
cytokine 36 33.24 Quite Low
Multiple sclerosis 19 5.00 Very Low Very Low Very Low
antagonist 11 5.00 Very Low Very Low Very Low
Hippocampus 10 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 459 100.00 Very High Very High Very High
Photosensitivity Disorders 2 98.80 Very High Very High Very High
Carcinoma 9 94.36 High High
Multiple Myeloma 4 89.80 High High
Death 117 89.12 High High
Cancer 257 84.08 Quite High
Fever 83 80.56 Quite High
Stress 43 78.20 Quite High
INFLAMMATION 94 76.20 Quite High
Parkinson's Disease 16 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Caspase-8, combined with its ability to induce apoptosis through the extrinsic pathway, also triggers the intrinsic apoptosis pathway by cleaving the pro-apoptotic Bcl-2 family members Bax and Bid to initiate mitochondrial-induced apoptosis [36-38].
Protein_catabolism (cleaving) of Bcl-2 associated with apoptosis
1) Confidence 0.64 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2577641 Disease Relevance 1.13 Pain Relevance 0.07
Bcl-2 cleavage and down-regulation of the inhibitor of apoptosis proteins (IAPs) family including cIAP-1/2, XIAP, and survivin, occurred downstream of ROS production during sulindac-induced apoptosis.
Protein_catabolism (cleavage) of Bcl-2 in cleavage associated with apoptosis
2) Confidence 0.56 Published 2007 Journal Apoptosis Section Abstract Doc Link 17136320 Disease Relevance 1.30 Pain Relevance 0.08
These results were correlated with caspase-3 and PARP cleavage and Bcl-2 degradation.
Protein_catabolism (cleavage) of Bcl-2 in cleavage
3) Confidence 0.16 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 1.56 Pain Relevance 0.15
These results were correlated with caspase-3 and PARP cleavage and Bcl-2 degradation.
Protein_catabolism (degradation) of Bcl-2 in cleavage
4) Confidence 0.16 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 1.56 Pain Relevance 0.15
Besides these cascades (green arrows), the caspase submodule is based on three mechanisms: i) autocatalytic events leading to the activation of many proteolytic enzymes that, once activated, greatly accelerate the degradation processes; ii) a feed-forward loop based on mitochondria and involving caspases and Bcl-2 family members (red arrows), and iii) a cross-talk between the extrinsic and intrinsic cascades (purple arrows).
Protein_catabolism (degradation) of Bcl-2
5) Confidence 0.04 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 0.14 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox